Research was conducted on the quasi-static in-service evaluation and long-term monitoring of bridge bearings through a field case study. The challenge with assessment of bearings, in their current state, is that the visual appearance is not a sufficient indicator of performance. In addition, bearings are difficult to monitor long-term in many cases due to their complex non-linearity. The motivation for evaluation and monitoring of these components is that they are critical to the long-term performance of bridges, particularly those with long-spans. At the service level, bearings accommodate thermal movements along with those from live load and wind effects. For extreme events, such as earthquakes, they dissipate energy and reduce the transfer of force into the superstructure. For the presented study, two primary objectives were established. The first was to evaluate the case study bridge bearings in their present state under service loads. Physics-based methods were evaluated using equilibrium and thermoelasticity. The second objective was to identify a long-term monitoring baseline. Artificial neural networks (ANNs) were explored due to the non-linear behavior present at two of the bearings. An ANN was trained with temperature changes to predict longitudinal bearing movement. The overall study illustrates potential techniques (with their limitations) for in-service evaluation and/or long-term monitoring of bridge bearings that have been assessed with structural health monitoring data.

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Effective energy expenditure is critical for maintaining body weight (BW). However, underlying mechanisms contributing to increased BW remain unknown. We characterized the role of brain angiogenesis inhibitor-3 (BAI3/ADGRB3), an adhesion G-protein coupled receptor (aGPCR), in regulating BW. A CRISPR/Cas9 gene editing approach was utilized to generate a whole-body deletion of the BAI3 gene (BAI3−/−). In both BAI3−/− male and female mice, a significant reduction in BW was observed compared to BAI3+/+ control mice. Quantitative magnetic imaging analysis showed that lean and fat masses were reduced in male and female mice with BAI3 deficiency. Total activity, food intake, energy expenditure (EE), and respiratory exchange ratio (RER) were assessed in mice housed at room temperature using a Comprehensive Lab Animal Monitoring System (CLAMS). While no differences were observed in the activity between the two genotypes in male or female mice, energy expenditure was increased in both sexes with BAI3 deficiency. However, at thermoneutrality (30 °C), no differences in energy expenditure were observed between the two genotypes for either sex, suggesting a role for BAI3 in adaptive thermogenesis. Notably, in male BAI3−/− mice, food intake was reduced, and RER was increased, but these attributes remained unchanged in the female mice upon BAI3 loss. Gene expression analysis showed increased mRNA abundance of thermogenic genes Ucp1, Pgc1α, Prdm16, and Elov3 in brown adipose tissue (BAT). These outcomes suggest that adaptive thermogenesis due to enhanced BAT activity contributes to increased energy expenditure and reduced BW with BAI3 deficiency. Additionally, sex-dependent differences were observed in food intake and RER. These studies identify BAI3 as a novel regulator of BW that can be potentially targeted to improve whole-body energy expenditure.

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SummaryStimulus-coupled insulin secretion from β-cells involves the fusion of insulin granules to the plasma membrane (PM) via SNARE complex formation—a cellular process key for maintaining whole-body glucose homeostasis. Optimal insulin secretion depends on how the clamping of SNAREs is released, rendering granules fusogenic. We show that an insulin granule protein synaptotagmin-9 (Syt9) deletion in lean mice increased glucose clearance, random-fed plasma insulin levels, and insulin secretion (in vivo and ex vivo islets) without affecting insulin sensitivity. These outcomes demonstrate that Syt9 has an inhibitory function in insulin secretion. Moreover, Syt9 interacts with PM-Stx1A and soluble Tomosyn-1 proteins to form non-fusogenic complexes between PM and insulin granules, preventing Stx1A-SNARE formation and insulin secretion. Furthermore, Syt9 inhibits SNARE-complex formation by posttranscriptional regulation of Tomosyn-1. We conclude that Syt9 and Tomosyn-1 are endogenous inhibitors that modulate Stx1A availability to determine β-cell secretory capacity.HighlightsSynaptotagmin-9 inhibits biphasic insulin secretion from β-cells.Synaptotagmin-9, syntaxin-1A, and Tomosyn-1 forms a molecular complex that decreases the availability of syntaxin-1A to form SNARE complexes in insulin secretion.Synaptotagmin-9–mediated inhibition of insulin secretion occurs through post-transcriptional regulation of Tomosyn-1.